Perspective:

The following are 10 points to remember from this overview of key concepts regarding atrial fibrillation (AF):

1. The primary goal of rhythm-control drug therapy is to prolong the refractory period in the atrium.

2. Targets for drug therapy that are atrial specific avoid the risk of ventricular proarrhythmia and consist of I_Kur and I_KACh.

3. Combination therapy with amiodarone plus ranolazine or dronedarone plus ranolazine has been shown experimentally to have marked synergistic effects that result in atrium-selective blockade of sodium channels and suppression of AF.

4. A potential target for drug therapy is endothelin 1, which modulates calcium recycling and promotes fibroblast proliferation.

5. Multiple inflammatory, oxidative stress, and vasoactive peptide markers (e.g., C-reactive protein and natriuretic peptides) are associated with AF, but it is unclear whether they are causally related to AF or epiphenomena.

6. The possible reasons why AF is more common in whites include underdiagnosis or competing risks in other racial groups, variable susceptibility to AF risk factors, and racial genetic differences.

7. Antithrombotic therapy with warfarin has been underutilized and it remains to be seen whether the utilization of antithrombotic therapy will improve with the availability of novel vitamin K antagonists such as dabigatran.

8. Angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers prevent atrial electrical and structural remodeling associated with AF, but the clinical evidence that these agents prevent AF is mixed.

9. Statins have anti-inflammatory, anti-ischemic, antioxidant, and antiarrhythmic effects that potentially could result in AF prevention, but the clinical results of statins for AF suppression have been mixed.

10. Moderate to severe sleep apnea is associated with a fourfold increase in the risk of AF.